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Cardio Renal II Final > Pharmacology - Arrhythmias Part 2 > Flashcards

Pharmacology - Arrhythmias Part 2 Flashcards

(75 cards)

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1
Q

true or false

class Ia sodium channel blockers have vagolytic properties and this is a positive effect

A

FALSE - negatve effect

vagolytic properties will result in increased heart rate and conduction which is udnesirable in arrhythmia patients

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2
Q

differentiate between the metabolism of procainamide/quinidine/disopyramide

A

procainamide goes directly to phase 2 acetylation to form NAPA

quinidine and disopyriamide undergo phase 1 by CYP3A4 — watch for DDI!!!!

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3
Q

true or false

quinidine slows conduction through the heart

A

true

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4
Q

true or false

quinidine can cause QT prolongation and thus torsades de pointes

A

true

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5
Q

name some unique AE of quinidine

A

cinchonism - tinnitus, headache, dizziness

also watch for low potassium (electrolytre imbalance) - contraindicated in hypokalemia

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6
Q

true or false

rifampin is a CYP3A4 inhibitor

A

FALSE - inducer

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7
Q

which class IA sodium channel blocker has the HIGHEST vagolytic activity

A

disopyramide

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8
Q

which 1A sodium channel blocker has similar anticholinergic side effects like atropine

A

disopyramide

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9
Q

disopyrimide is only given in….

A

LIFE THREATENING ventricular arrhythmia

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10
Q

CI disopyramide

A

may cause or worsen CHF! or severe hypotension

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11
Q

name 2 types of drugs that quinidine is CI with

A

drugs that prolong QT or drugs that cause electrolyte imbalance (specifically hypokalemia)

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12
Q

true or false

lidocaine blocks both activated and inactivated sodium channels with rapid kinetics

A

true

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13
Q

lidocaine is highly effective in what specific arrhythmias

A

those associated with acute MI

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14
Q

explain HOW lidocaine is an antiarrhythmic

A

increases the threshold

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15
Q

true or false

lidocaine is most effective on atrial cells

A

FALSE - greater effects on cells with long action potentials like purkinje and ventricular cells

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16
Q

true or false

lidocaine can be given oral or IV

A

FALSE - only IV

extensive 1st pass

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17
Q

explain lidocaine dose adjustments

A

its highly protein bound to alpha acid glycoprotein - need to MONITOR and adjust dose accordingly to prevent AE

decrease the dose in drugs like propranolol that decrease liver perfusion and thus decrease metabolism

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18
Q

metabolism of lidocaine

A

1A2 AND 3A4

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19
Q

CI lidocaine

A

in patients with preexisting condction abnormalities like SA, AV block

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20
Q

true or false

lidocaine is one of the LEAST cardiotoxic sodium channel blockers

A

TRUE !!!! weakly bound - fast dissociation kinetics

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21
Q

can lidocaine cause hypotension

A

yes - by depressing contractility

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22
Q

true or false

lidocaine does not have CNS AE

A

FALSE - it does

bc of the hypotension can cause lightheadedness and also sodium channel blocking in general

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23
Q

lidocaine plasma levels should be kept below ____ to avoid side effects

A

9 micrograms/mL

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24
Q

true or false

mexiletine is given orally

A

true

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25
metabolism of mexiletine
CYP2D6
26
general AE mexelitine
CNS (like lidocaine) tremor, blurred vision, etc
27
effect of flecainide on APD
DOES NOT PROLONG
28
true or false flecainide has SLOW unbinding kinetics
true
29
true or false out of all of the Na channel blocking classes, flecainide has the most anticholinergic effects
FALSE - has no anticholinergic effects!
30
metabolism of flecainide
2d6
31
is flecainide given orally
yes
32
in which patients can class IC sodium channel blockers NOT BE GIVEN TO
patients with structural heart disease!!!!!!!!!!!!! higher mortality
33
true or false flecainide is proarrhythmogenic
true
34
unique mechanism of propafenone
structurally similar to propranolol so has weak beta blocking action!!
35
DDI concerns propafenone
3A4 AND 2D6 inducers/inhibitors also increases concentrations of digoxin, warfarin, and propranolol! need to decrease their doses!
36
name 5 class 3 potassium channel blockers/multichannel blockers
amiodarone dronedarone dofetilide sotalol ibutilide
37
major effect of class 3
increased APD and ERP (effective refractory period)
38
true or false no 1C sodium channel blockers should be used in heart disease patients
true
39
true or false class III blocks repolarization
TRUE blocks potassium channels in phase 3 -- preventing repolarization
40
true or false class III shortens the ERP
FALSE - prolongs
41
true or false class III does not show reverse use dependence
FALSE - it does
42
what does it mean that potassium channel blockers show reverse use dependance
effect is low at higher heart rates (higher heart rate is when the action is really needed!!!)
43
true or false ALL class III causes QT prolongation
true
44
what does amiodarone structurally resemble
thyroxine (T4)
45
explain the hydrophilic/lipophilic properties of amiodarone
VERY LIPOPHILIC!!! accumulates in adipose and thyroid tissue and can cause toxicity to increase absorption, take with food!!!
46
name a scenario in which amiodarone has been shown to benefit patients
shown to decrease the frequency of cardioverter-defibrillator discharges (shock delivered to heart_
47
true or false amiodarone is widely used and useful against most arrhythmias
true
48
**true or false the major action of amiodarone is as a class III potassium channel blocker
TRUE minor action is sodium channel blocking
49
in what state does amiodarone block sodium channels
in the inactivated state
50
true or false amiodarone shows NO reverse use dependence
true
51
true or false amiodarone does not cause QT prolongation
false - all the class III do. however, risk of torsades is low
52
does amiodarone have any effects outside of the heart?
YES - causes vasodilation and decreased blood pressure when given IV
53
route of administration amiodarone explain how route changes the action
oral and IV oral - takes 1-3 weeks to see effect. usually more used for prevention IV - you see rapid effects. usually used for treatment
54
true or false amiodarone has a low Vd
FALSE - high Vd. accumulates in adipose and thyroid tissue
55
excretion of amiodarone
biliary (fecal)
56
true or false amiodarone has a short half life
FALSE - very long. takes several weeks for the action of the drug to stop
57
DDI concerns with amiodarone
metabolized by 3A4!
58
amiodarone + statin
increased statin levels and thus increased risk of myopathy
59
cyclosporine/digoxin + amiodarone
increased levels of cyclosporine/digoxin bc amiodarone inhibits Pgp (efflux protein) digoxin dose needs to be decreased by half!
60
5 things that INHIBIT CYP3A4 and thus increase toxicity of amiodarone
"CLAP G" cimetidine loratidine antidepressent (trazodone) protease inhibitors grapefruit juice
61
2 CYP3A4 inducers what is their effect on amiodarone
rifampin and st john's wort decreased efficacy of amiodarone
62
3 drugs that increase risk of QT prolongation when given with amiodarone
azole antifungals macrolides fluoroquinolones
63
fentanyl/lidocaine/dextromethorphan + amiodarone
increase levels of fentanyl/lidocaine/DM
64
cholestyramine + amiodarone
decreased amiodarone levels (only applies to oral!)
65
mechanism of amiodarone thyroid toxicity
blocks conversion of T4 to T3 (active) - hypothyroidism (WOLFF-CHAIKOFF EFFECT) or hyperthyroidism
66
areas with high diet of iodine + amiodarone...
hyperthyroidism
67
amiodarone toxicities
thyroid toxicity skin gray-blue discoloration loss of vision pulmonary toxicity bradycardia worsened arrhythmias
68
structural analog of amiodarone
dronedarone
69
differences between amiodarone and dronedarone
the iodine was removed has NO EFFECT on thyroxine metabolism like amiodarone does
70
true or false dronedarone doesnt accumulate as much as amiodarone
true - shorter half life
71
true or false unlike amiodarone, dronedarone has NO thyroid effects and NO pulmonary toxicity
true
72
true or false dronedarone has liver toxicity
true
73
DDI concern with dronedarone
cyp3a4 substrate and inhibitor
74
BBW of dronedarone
DO NOT USE IN HEART FAILURE PATIENTS
75

Cardio Renal II Final (11 decks)

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